Kathleen Sarmiento

Update in sleep medicine 2012.

In obstructive sleep apnea (OSA), the upper airway recurrently collapses during sleep due to an imbalance in forces that usually maintain pharyngeal patency. Given the importance of upper airway motor control, Saboisky and colleagues sought to confirm the presence of neurogenic changes and quantify the extent of neural remodeling in hypoglossal nerve branches (1). In this study of 31 patients, 17 of whom had OSA, genioglossus EMG signals and motor unit potential trains were extracted and analyzed quantitatively. This study revealed that the genioglossus motor unit potential trains were longer in duration and larger in size index in patients with OSA versus control subjects, strong indicators of neurogenic change. These changes were attributed to motor unit remodeling from denervation, collateral sprouting, and reinnervation and were associated with the severity of hypoxemia during sleep. In an accompanying editorial, Levy and colleagues suggested that the cross-sectional study design did not allow separation of cause and effect (2). Although pharyngeal neuropathy might be a consequence of SDB, it may also perpetuate OSA. The authors acknowledged that more studies are required regarding these neurogenic changes. Given the evidence for hypoglossal neurogenic dysfunction in OSA, specific treatment modalities such as hypoglossal nerve stimulation (HGNS) may have a therapeutic role. HGNS is potentially efficacious in patients with OSA intolerant of continuous positive airway pressure (CPAP) (3). Schwartz and colleagues sought to determine if the efficacy of HGNS was due to its ability to improve airflow and to relieve airway obstruction (4). This study of 30 patients with OSA found that HGNS produced marked doserelated increases in airflow without arousal from sleep. Although all patients achieved near-normal flow with HGNS, patients with persistent inspiratory airflow limitation required higher stimulus intensity to achieve peak flow, suggesting this subset of patients needed recruitment of other pharyngeal dilator muscles. Overall, the authors believed their findings supported the need for further research into HGNS, including awaiting the results of multiple ongoing multinational randomized trials, although early unpublished reports have been disappointing.

Treatment of OSA with CPAP Is Associated with Improvement in PTSD Symptoms among Veterans.

STUDY OBJECTIVES Posttraumatic stress disorder (PTSD) is common among veterans of the military, with sleep disturbance as a hallmark manifestation. A growing body of research has suggested a link between obstructive sleep apnea and PTSD, potentially due to obstructive sleep apnea (OSA) related sleep disruption, or via other mechanisms. We examined the hypothesis that treatment of OSA with positive airway pressure would reduce PTSD symptoms over 6 months. METHODS A prospective study of Veterans with confirmed PTSD and new diagnosis of OSA not yet using PAP therapy were recruited from a Veterans Affairs sleep medicine clinic. All subjects were instructed to use PAP each night. Assessments were performed at 3 and 6 months. The primary outcome was a reduction in PTSD symptoms at 6 months. RESULTS Fifty-nine subjects were enrolled; 32 remained in the study at 6 months. A significant reduction in PTSD symptoms, measured by PCL-S score was observed over the course of the study (60.6 ± 2.7 versus 52.3 ± 3.2 points; p < 0.001). Improvement was also seen in measures of sleepiness, sleep quality, and daytime functioning, as well as depression and quality of life. Percentage of nights in which PAP was used, but not mean hours used per night, was predictive of improvement. CONCLUSIONS Treatment of OSA with PAP therapy is associated with improvement in PTSD symptoms, although the mechanism is unclear. Nonetheless, PAP should be considered an important component of PTSD treatment for those with concurrent OSA. Improving PAP compliance is a challenge in this patient population warranting further investigation. CLINICAL TRIAL REGISTRATION ClinicalTrials.gov, ID: NCT02019914. COMMENTARY A commentary on this article appears in this issue on page 5.

Original InvestigationEditorial CommentObstructive Sleep Apnea and Atrial Fibrillation: Is the Link Real?∗

Increasingly compelling data link obstructive sleep apnea (OSA) to cardiovascular impact, independent of known comorbidities [(1)][1]. OSA is estimated to affect ∼10% of individuals [(2)][2], a figure that has been increasing due to the obesity pandemic and an aging population, both of which

Obstructive sleep apnea and atrial fibrillation: Is the link real?

Increasingly compelling data link obstructive sleep apnea (OSA) to cardiovascular impact, independent of known comorbidities [(1)][1]. OSA is estimated to affect ∼10% of individuals [(2)][2], a figure that has been increasing due to the obesity pandemic and an aging population, both of which

ATS Core Curriculum 2016: Part I. Adult Sleep Medicine

Jay S. Balachandran, Columbia St. Marys Hospital Carey C. Thomson, Mount Auburn Hospital Dezmond B. Sumter, University of Michigan Anita V. Shelgikar, University of Michigan Philippe Lachapelle, McGill University Health Centre Sushmita Pamidi, McGill University Health Centre Michael Fall, Medical University of South Carolina Chitra Lal, Medical University of South Carolina Ridhwan Y. Baba, Case Western Reserve University Neomi Shah, Icahn School of Medicine at Mount Sinai

Mechanisms and implications of the link between sleep apnoea and chronic kidney disease

See article, page 754

Stimulating progress in the upper airway

851 Editorial—Orr et al. Pathogenesis of obstructive sleep apnea (OSA) is multifactorial and largely due to anatomic predisposition, ventilatory control abnormalities, and ineffective pharyngeal dilator muscles.1 Gold standard treatment for OSA is continuous positive airway pressure (CPAP), which provides a pneumatic splint of the upper airway. While impressively efficacious, CPAP use in the real world suffers from the same 50% compliance ceiling that plagues treatments of many other chronic diseases.2 There has been a call within the sleep field to develop alternate treatment options not only to improve compliance, but also to personalize the approach to therapy. An intervention targeting specific pathogenic mechanisms of OSA, such as ineffective upper airway dilator muscles, offers the appeal of tailored therapy rather than a one-size-fits-all approach. In this month’s issue of SLEEP, Dedhia and colleagues3 review 25 years of progress in upper airway stimulation (UAS), including the multitude of proof-of-concept animal and human studies, which contributed to the recent FDA approval of this therapy. The authors are commended on their excellent review of the historical proof-of-concept studies leading to the recent randomized clinical trials of UAS therapy. Understanding the basis for this new therapeutic is critical in promoting acceptance and understanding of its role in the sleep physician’s armamentarium. Their review by Dedhia et al.3 addresses commonly asked questions, including why unilateral lead placement suffices; whether this single lead results in concentric contraction of airway dilator muscles; whether multi-level activation of pharyngeal dilator muscles occurs; and what the role is of inspiratory gating for this device. One of the most interesting facets of this review is the discussion of the effectiveness of this device to address airway collapsibility at multiple levels, a novel departure from most other surgical interventions for OSA. Moreover, the steps involved in implantation of these stimulators are thoroughly described in the review.3 Given the fact that the device is not yet widely available, most readers of this review will benefit from these historical and current perspectives. The approach to treating patients with OSA is complex and involves consideration of several available treatment modalities in concert with preferences of the patient. Compliance EDITORIAL